Consultation appointment Shi Shurong: Why did the doctor prescribe targeted drugs as soon as the diagnosis of chronic myeloid leukemia was confirmed?

The current treatment of chronic myeloid leukemia is mainly based on tyrosine kinase inhibitors (targeted drugs). The first-generation drugs commonly used in clinical medicine are imatinib, the second-generation drugs nilotinib and dasatinib, and the third-generation drugs are also available. Listed abroad. Different development periods require different medications and dosages. Director Shi Shurong’s WeChat consultation platform: zkxk9999 why tyrosine kinase inhibitors can effectively treat chronic myeloid leukemia? The formation of Ph chromosome in patients with chronic myeloid leukemia produces the BCR-ABL fusion gene, whose encoded product has sustained tyrosine kinase activity and activates downstream signaling pathways leading to the occurrence of CML. Tyrosine kinase inhibitor TKI can be used as a competitive inhibitor of adenosine triphosphate (ATP) binding to tyrosine kinase, or as a tyrosine analog, blocking the activity of tyrosine kinase, inhibiting the proliferation of tumor cells and inducing tumors Cell apoptosis plays an anti-tumor effect. In the process of medication, the above drugs can competitively bind to ATP with BCR-ABL fusion protein, inhibit its tyrosine kinase activity and its downstream signaling to play an anti-leukemia effect. The treatment goal of chronic myeloid leukemia: first of all, the disease should be controlled in the chronic stage as much as possible to prolong the life of the patient. On the basis of prolonging survival, improving the quality of life and living like a normal person has become the demand of CML patients. It is our ultimate goal to “cure” CML without continuous remission without treatment. Slow-grain patients can self-examine and evaluate the treatment goals: first, complete hematological remission, that is, normal blood routine, symptoms and splenomegaly disappear; second, complete cytogenetic response within 12 months, that is, the Ph chromosome cannot be detected ; Get the main molecular response again within 18 months, namely BCR-ABL quantitative (IS, international standardization) &lt.0.1%, get the deepest molecular response as much as possible. It should be noted that slow-grain patients are not allowed to stop taking drugs when taking targeted drugs. Even if the evaluation of the therapeutic effect is the best response, they need to be gradually reduced according to the doctor’s instructions until the drug is stopped, so as to avoid sudden rebound and even worsen the condition. More patient communication assistance can follow the WeChat public account [Slow Grain Patient Association] mbxb120

Explaining why JAK2 gene mutation causes “true red”? Shi Shurong explained

Polycythemia vera (PV), or “true red” for short, is a bone marrow proliferative tumor (MPN) that originates from hematopoietic stem cells. The main manifestation is a myeloproliferative tumor characterized by abnormally increased red blood cells and independent of the normal erythropoiesis regulation mechanism. Director Shi Shurong’s micro-signal xueyeke999JAK2 gene can be seen in almost all patients with true red. It is an important diagnosis. JAK2 (Janus kinase 2) is a member of the 4 members of the JAK family (TYK2, JAK1, JAK2, JAK3) and is a non-receptor Peptide kinase (PTK), located on the short arm of chromosome 9 (9p24), plays an important role in the regulation of hematopoiesis. JAK2 gene point mutation occurs in exon 14 of JAK2 gene 1849, that is, the base of codon 617 of JAK2 gene coding sequence is G-T transposed, so that the original guanine G is replaced by thymine T, The valine encoded by it becomes phenylalanine. JAK2V617F is a somatic function acquired mutation that occurs at the level of hematopoietic stem/progenitor cells. When JAK2V617F mutation occurs, even in the absence of EPO, it can cause the continuous activation and enhancement of JAK2 kinase and downstream signal transduction pathways, resulting in Inhibition of malignant cell proliferation and apoptosis eventually causes the occurrence of PV. In addition, JAK2V617F mutation can also induce activation and signaling abnormalities of thrombopoietin receptor (TPOR) and granulocyte colony stimulating factor receptor (G-CSFR), resulting in abnormal proliferation of megakaryocyte cell lines and granulocyte progenitor cells, ET and The incidence of PMF may also be related to this. JAK2 gene mutations are ubiquitous in PV patients, and JAK2V617F mutation-negative PV patients often have other types of mutations related to the JAK2 gene, especially JAK2 exon 12 mutations. In addition, it also includes: DNMT3a, ASXL1, TET2, IDH1/2 and other gene mutations. These mutations not only lead to abnormal proliferation of the erythroid system, but also abnormal proliferation of the granulocyte and megakaryocytic system, and may constitute the molecular mechanism of PV progression to myelofibrosis and acute leukemia. For more erythrocytosis disease knowledge or patient help, you can pay attention to WeChat public number: zkxy120

Shi Shurong’s consultation number appointment: slow granules achieve good results, and doctor-patient cooperation is also crucial!

Clinically, according to the progression of chronic myeloid leukemia, it can be divided into three development periods, namely: chronic period, accelerated period and acute change period. Among them, the treatment in the chronic phase is very critical for patients with chronic granules. Effective treatment measures are taken early and in a timely manner, and the condition is easily controlled. Director Shi Shurong’s traditional treatment and targeted therapy of WeChat xueyeke999 chronic myeloid leukemia are mainly chemotherapy (hydroxyurea, etc.), interferon and hematopoietic stem cell transplantation. At first, chronic myeloid leukemia, like other types of leukemia, was regarded as an incurable disease. Under the condition that hydroxyurea and interferon are not ideal, it is believed that only bone marrow transplantation can “cure” the disease. With the application of targeted drugs such as tyrosine kinase inhibitors (TKI), the treatment of chronic myeloid leukemia has made great progress, and the survival period has been extended to 15-20 years, or even longer. Targeted therapies for BCR/ABL tyrosine kinase include first-line therapy imatinib, second-line drugs nilotinib and dasatinib, while treatment failure for second-generation tyrosine kinase inhibitors, or concomitant In patients with resistance mutations such as T315I, allogeneic hematopoietic stem cell transplantation may be the most appropriate treatment option. Judgement and monitoring of therapeutic effects The diagnosis and treatment goals of chronic myeloid leukemia have been not only to obtain hematological and genetic remission (chromosome conversion), but more importantly to achieve molecular remission (BCR/ABL gene conversion), only to obtain a good molecular response Patients can survive long-term. Therefore, closely monitoring changes in chromosomes and BCR/ABL fusion genes is an important basis for judging the efficacy and selection of treatment. If these tests are neglected, the patient may not be able to understand the changes in the disease in a timely manner, and the medication regimen may be adjusted accordingly, which may also lead to treatment failure! In addition to treatment options, doctor-patient cooperation is the key to better results! The patient’s compliance and the degree of cooperation with the treatment will also affect the treatment effect. Therefore, strengthening the communication between patients with disease knowledge and treatment information can increase the patient’s knowledge of the disease and improve the patient’s cooperation with the treatment, which is conducive to the doctors and patients working together to overcome the disease. It can be seen that patients with chronic myeloid leukemia want to achieve good results. They must choose the appropriate treatment method, control the disease in a timely manner, and understand how to cooperate with the doctor’s treatment. There is also regular review and monitoring of efficacy. Every link is very good. The essential. For more knowledge about chronic myeloid leukemia disease or patient help, please pay attention to WeChat public account: mbxb120